In addition, insulin stimulates hepatic lipase, which facilitates the uptake of free fatty acids derived from gut chylomicron remnants into the liver. FFAs are subsequently esterified into triglycerides, and then packaged into VLDL particles that are exported and stored in other tissues as an additional JQ-1 carboxylic acid energy substrate. During growth and development there are fluctuating demands for energy substrates as well as dramatic changes in nutrition, as offspring transition from fetus to postnatal life, and from pre- to post-weaning. In utero, the main energy substrate transferred across the placenta is glucose. However, after birth there is a sudden change in energy substrate availability due to the consumption of high-fat, low-carbohydrate milk. Thus, a metabolic adaptation at birth is necessary to maintain blood glucose levels. In rodents, this adaptation is accomplished by activation of gluconeogenic, lipid oxidative, and ketogenic pathways. The suckling-weaning transition is also accompanied by a profound change in nutrition. As weaning approaches, milk intake is gradually replaced by intake of higher-carbohydrate, lower-fat, solid foods. To ensure Idalopirdine hydrochloride survival, neonates must successfully adapt to these changes in nutrition throughout development, which requires significant changes in energy substrate metabolism. Thus, hepatic energy metabolism is dynamically regulated throughout different life stages. However, mechanisms governing this regulation are not completely understood. The purpose of this study is to provide a comprehensive quantification of the mRNA abundance of energy metabolism genes during liver development. To accomplish this, we used RNA-Sequencing, which has the distinct advantage of enabling us to determine the true quantification of transcripts, and is not delimited by the requirement for primers or probes as is the case with other mRNA detection tools such as Northern blotting, PCR, or DNA microarray. Using mouse ontogenic development as a tool, we hope to gain a better understanding of the developmental regulation of energy metabolism genes, which may lead to novel therapeutic targets for pathologies associated with aberrant metabolic gene regulation.